In vivo response to initial therapy, as assessed by determination of minimal residual disease (MRD) after 5 and 12 weeks of treatment, has evolved as a strong prognostic factor in children with acute lymphoblastic leukemia (ALL) treated according to the BFM regime. Individual treatment response may be influenced by copy number alterations (CNA) leading to altered gene expression. We aimed to evaluate CNA using high-resolution array-comparative genomic hybridization (array-CGH) in different treatment-response groups. Leukemic genomic profiles of 25 standard risk (MRD-SR) and 25 high risk (MRD-HR) patients were compared. CNAs were found in 46/50 patients (92%). The most significant difference was a gain of 1q23-qter because of an unbalanced t(1;19), found in 10/25 MRD-SR patients, but in none of the MRD-HR patients (P < 0.001). The most frequent CNAs in the MRD-HR group were deletions of genomic regions harboring the immunoglobulin genes (Ig), e.g., 2p11.2 in 60% of MRD-HR compared to 28% of MRD-SR (P = 0.045). Combining all Ig loci, significantly more MRD-HR than MRD-SR patients displayed deletions (17:8 patients, P = 0.02). Frequency of other CNAs, such as loss of 9p21 or gains of 21q, did not differ strongly between the two patient groups. This is the first study evaluating the clinical significance of CNA as detected by array-CGH in childhood ALL and the first to suggest that such analyses may provide clinically important data. This article contains supplementary material available via the Internet at http://www.interscience.wiley.com/jpages/1045-2257/suppmat.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1002/gcc.20557 | DOI Listing |
Front Plant Sci
December 2024
Department of Plant Pathology, North Dakota State University, Fargo, ND, United States.
Soybean cyst nematode (SCN, ) is a devastating pest affecting soybean production worldwide. Host resistance is one of the primary practices used to manage SCN. The locus contributes to the strong and effective SCN resistance, with resistance levels predominantly governed by copy number variations (CNVs) and, to lesser extent, sequence variations.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Hearing loss (HL) is the most common sensory disorder, characterized by a wide range of causes, including both environmental and genetic factors. While single-nucleotide variants (SNVs) and small insertions/deletions have been extensively studied, the role of structural variations (SVs) in hearing impairment has gained increasing recognition. This review article aims to provide a comprehensive overview of the importance of SVs in HL, by exploring the SVs associated with HL and their underlying pathogenic mechanisms.
View Article and Find Full Text PDFJ Med Virol
January 2025
The Wistar Institute, Philadelphia, Pennsylvania, USA.
Epstein-Barr virus (EBV) is a ubiquitous human ɣ-herpesvirus implicated in various malignancies, including Burkitt's lymphoma and gastric carcinomas. In most EBV-associated cancers, the viral genome is maintained as an extrachromosomal episome by the EBV nuclear antigen-1 (EBNA1). EBNA1 is considered to be a highly stable protein that interacts with the ubiquitin-specific protease 7 (USP7).
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Zoology, The University of Burdwan, Bardhaman, West Bengal, 713104, India.
Background: This study aimed to develop and validate a targeted next-generation sequencing (NGS) panel along with a data analysis algorithm capable of detecting single-nucleotide variants (SNVs) and copy number variations (CNVs) within the beta-globin gene cluster. The aim was to reduce the turnaround time in conventional genotyping methods and provide a rapid and comprehensive solution for prenatal diagnosis, carrier screening, and genotyping of β-thalassemia patients.
Methods And Results: We devised a targeted NGS panel spanning an 80.
Cancer Discov
January 2025
Memorial Sloan Kettering Cancer Center, New York, NY, United States.
The role of ubiquitin-mediated degradation mechanisms in the pathogenesis of diffuse large B cell (DLBCL) and follicular lymphoma (FL) is not completely understood. We show that conditional deletion of the E3 ubiquitin ligase Fbxo45 in germinal center B-cells results in B-cell lymphomagenesis in homozygous (100%) and heterozygous (48%) mice. Mechanistically, FBXO45 targets the RHO guanine exchange factor ARHGEF2/GEF-H1 for ubiquitin-mediated degradation.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!